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. 2021 Apr 8;23(4):540–548. doi: 10.1007/s12017-021-08656-0

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — IL-2/IL-2R treatment increases Treg-induced survival of NPCs and reduction of inflammation. Left panel: OGD/R reduced cell viability of NPCs but was significantly blocked by IL-2/IL-2R-Treg treatment and Treg treatment (*p < 0.0001), while cell survival with IL-2/IL-2R treatment alone was comparable to that of the media control treatment group (p > 0.05). IL-2/IL-2R-Treg treatment was found to be significantly greater than with Treg treatment alone (*p < 0.0001). Right panel. OGD/R elevated TNF-α levels which was significantly suppressed by IL-2/IL-2R-Treg treatment (*p < 0.0001) or Treg treatment alone (*p < 0.0001), while IL-2/IL-2R treatment alone was ineffective in inhibiting TNF-α levels, comparable to that of the media control treatment group (p > 0.05). TNF-α levels with IL-2/IL-2R-Treg treatment were found to be significantly lower than Treg treatment alone (**p < 0.005). Under ambient condition (i.e., without OGD/R), only trace TNF-α levels were detected